Titlebook: Retinal Degenerative Diseases; Mechanisms and Exper Catherine Bowes Rickman,Matthew M. LaVail,John Ash Conference proceedings 2016 The Edit

Polydipsia

Biology of p62/sequestosome-1 in Age-Related Macular Degeneration (AMD)nflammation, apoptosis, and autophagy. Our previous work has revealed in the retinal pigment epithelium (RPE) that p62 promotes autophagy and simultaneously enhances an Nrf2-mediated antioxidant response to protect against acute oxidative stress. Several recent studies demonstrated that p62 contribu

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Gene Structure of the 10q26 Locus: A Clue to Cracking the ARMS2/HTRA1 Riddle?itizens, it represents a major public health issue in developed countries. Genetic studies of AMD identified two major susceptibility loci on chromosomes 1 and 10. The high-risk allele of the 10q26 locus encompasses three genes, PLEKHA1, ARMS2, and HTRA1 with high linkage disequilibrium and the indi

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Conditional Induction of Oxidative Stress in RPE: A Mouse Model of Progressive Retinal Degenerationes to the pathological changes of the retinal pigment epithelium (RPE), we are reporting a new mouse AMD model of retinal degeneration by inducing mitochondrial oxidative stress in RPE. . the gene for manganese superoxide dismutase (MnSOD) was deleted in RPE layer using conditional knockout strategy

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A Brief Discussion on Lipid Activated Nuclear Receptors and their Potential Role in Regulating Micron World. A common morphological denominator in all forms of AMD is the accumulation of microglia within the sub-retinal space, which is believed to be a contributing factor to AMD progression. However, the signaling pathway and molecular players regulating microglial recruitment have not been comple

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Ganglion-Cyst

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Oxidative Stress and the Nrf2 Anti-Oxidant Transcription Factor in Age-Related Macular Degeneration dry form of the disease (dAMD) for which reliable therapies are lacking. A major obstacle to the development of effective treatments is a deficit in our understanding of what triggers dAMD onset. This is particularly the case with respect to the events that cause retinal pigment epithelial (RPE) ce

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Aging Changes in Retinal Microglia and their Relevance to Age-related Retinal Diseaseromote disease progression. However, the relationship between aging and neuroinflammation is unclear. Microglia are long-lived, resident immune cells of the retina, and mediate local neuroinflammatory reactions. We hypothesize that aging changes in microglia may be causally linked to neuroinflammato

Melanoma

VEGF-A and the NLRP3 Inflammasome in Age-Related Macular Degenerationivated in the retinal pigment epithelium (RPE) in eyes with AMD. However, it is not known whether inflammasome activation is a cause or consequence of pathologic changes in AMD. A roadblock to defining the role of inflammasome activation and pathways that regulate it for AMD has been the lack of a m